Host resistance to cancer almost certainly involves multiple immunospecific and nonspecific mechanisms, yet despite impressive tumoricidal activity in vitro, effector cells in vivo seem unable to cope with neoplastic cells after they have emerged as a discrete tumor. We have evidence that neoplastic development inhibits macrophage accumulation at inflammatory sites. This situation is not unique to cancer, as a similar disturbance follows major surgery and local inflammation. By cross-desensitization experiments, however, we showed that the mechanism of macrophage inhibition that follows major surgery is analogous to that induced by local inflammation but distinguished from that induced by cancer. In a separate study, we noted that a variety of methods have been described to measure cytotoxicity of host effector cells. While these methods have proven their value, they have certain limitations--most notably that the measured parameter cannot be related to the overall rate of tumor growth. Over the past 3 years, we have developed a cytokinetic assay of cytotoxicity based upon rates of target cell loss and replication. Cytolysis by BCG-activated macrophages in vitro was insufficient to arrest P-815 mastocytoma growth. The latter required a prolongation in replication rate, as well as a decrease in survival rate. Collectively, our studies address the issue as to how cancer cells avoid destruction by host effector cells by exploring the parameters that influence the effectiveness of host resistance mechanisms. (SR)